Examining the mutational landscape in 439 non-smoker lung cancers a higher frequency in high (i.e., >45 Bq/m3) vs. low exposed Radon patients was found for mutations targeting the DNA damage response/repair machinery (ATR, ATRX, BARD1, RAD50, and SMARCA4), histonedeacetylase2 (HDAC2), and inhibitor of nuclear factor kappaB kinase subunit epsilon (IKBKE), as well as EGFR- and TP53 [52]. This evidence concerns the gene EGFR and lung carcinoma.